Left ventricular strain and transmural structural remodeling distribution in hypertensive heart disease

Abstract

Left ventricular (LV) systolic wall strain is one of the new candidates for the prognostic indicator for the hypertensive heart failure. However, it is still unclear what underlying transmural structural remodeling corresponds strain abnormality in progression of hypertensive heart failure. Objective and methods: To investigate the relationship between the structural change and myocardial strain, 60 Dahl salt-sensitive rats fed a high-salt (HF-group) or a low-salt diet (Control-group) from 6-weeks age. Pressure-volume relationship was analyzed and lung weight was measured at 10, 14, and 18 weeks of age and assessed the heart failure stage. In each stage, transmural distribution of LV myocardial fiber angle, fibrosis, and myocyte hypertrophy were evaluated pathologically and related mRNA quantification were performed. LV global longitudinal (GLS) and circumferential strain (GCS) were measured using 2D speckle tracking echocardiography. Results: While, Emax was preserved throughout the study period, tau and EDPVR indicated progressive deterioration from 14 weeks (diastolic dysfunction stage). And lung weight was significantly increased at 18 weeks (decompensated stage). Myocardial fiber orientation did not change as disease progress. Fibrosis-area% in histology and collagen type I/ type III mRNA ratio were significantly elevated in subendocardial-layer at 14 weeks and propagated into mid-layer at 18 weeks. Myocyte hypertrophy and mRNA of embryonic type -myosin heavy chain increased in subendocardial-layer at 14 weeks and progress into mid-layer at 18 weeks. In compared to control-group, HT-group showed progressively deteriorated GLS at 14 weeks (-27±4% in control, -17±3% in HT-group, p<0.001) and GCS decreased at 18 weeks (-27±3% in control, -17±2% in HT-group, p=0.002) Conclusions; LV wall strain alternations were accompanied by transmural progression of fibrosis and hypertrophy, and GLS related to subendocardial-layer remodeling, and GCS corresponded to mid-layer involvements.